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Titolo:
Post-junctional mechanisms involved in the potentiation of cardiac adrenergic responses by cocaine
Autore:
Sabra, R; Khoury, HA; Bechara, G; Sharaf, LH; El-Bizri, NM;
Indirizzi:
Amer Univ Beirut, Fac Med, Dept Pharmacol & Therapeut, Beirut, Lebanon Amer Univ Beirut Beirut Lebanon Pharmacol & Therapeut, Beirut, Lebanon
Titolo Testata:
EUROPEAN JOURNAL OF PHARMACOLOGY
fascicolo: 1, volume: 397, anno: 2000,
pagine: 139 - 150
SICI:
0014-2999(20000526)397:1<139:PMIITP>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
CENTRAL-NERVOUS-SYSTEM; SYMPATHETIC NEURAL ACTIVITY; NEURONAL MONOAMINE UPTAKE; VENTRICULAR-FIBRILLATION; ANESTHETIZED DOGS; CALCIUM; RATS; STIMULATION; PROTECTION; RABBITS;
Keywords:
cocaine; potentiation; noradrenaline; blood pressure; contractility; chlorisondamine;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
42
Recensione:
Indirizzi per estratti:
Indirizzo: Sabra, R Amer Univ Beirut, Fac Med, Dept Pharmacol & Therapeut, POB 11-0236-37, Beirut, Lebanon Amer Univ Beirut POB 11-0236-37 Beirut Lebanon Beirut, Lebanon
Citazione:
R. Sabra et al., "Post-junctional mechanisms involved in the potentiation of cardiac adrenergic responses by cocaine", EUR J PHARM, 397(1), 2000, pp. 139-150

Abstract

Cocaine cardiotoxicity is partly due to sympathetic activation of the heart resulting from inhibition of catecholamine uptake at the sympathetic nerve terminal and possible central sympathetic stimulation and/or inhibition. This study evaluated the role of postsynaptic mechanisms in potentiation bycocaine of cardiac adrenergic responses. Cardiovascular responses (arterial and left ventricular pressure, contractility and heart rate) to increasing doses of noradrenaline and to isoproterenol were obtained in anesthetizedcats during a control period, after irreversible or-adrenoceptor blockade with phenoxybenzamine (5 mg/kg i.v.), and after cocaine (5 mg/kg, i.v.). Responses to noradrenaline were significantly reduced by phenoxybenzamine with lowering of the maximal rise of all parameters. Cocaine shifted the dose-response curve of noradrenaline to the left and enhanced its maximal effects. Some responses to isoproterenol, which is not taken up by nerve terminals, were also enhanced by cocaine. Pretreatment with chlorisondamine or verapamil prevented the cocaine-induced enhancement of the maximal response to noradrenaline and the response to isoproterenol, but it did not inhibit potentiation of submaximal doses. Lidocaine did not potentiate the response tonoradrenaline or isoproterenol. Use of chlorisondamine instead of cocaine potentiated responses to all noradrenaline doses and enhanced the responsesto isoproterenol. These results suggest that the potentiation by cocaine of cardiac responses to adrenergic stimuli involves presynaptic mechanisms to block noradrenaline re-uptake, and postsynaptic mechanisms to raise the maximal responses. The latter may result from inhibition of central sympathetic outflow or from activation of cardiac Ca+ channels, leading to increased cardiac sensitivity to noradrenaline. (C) 2000 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/01/20 alle ore 14:35:45